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3.4.1.3 Congenital Rubella Infection andHearing Loss
Rubella virus is an enveloped single-stranded RNA virus. It may cause intrauterine rubella infection when contracted during pregnancy, resulting in many clinical consequences ranging from asymptomatic infection to miscarriage or stillbirth
or congenital birth anomalies, named congenital rubella syndrome. Because
rubella is a vaccine-preventable illness, congenital rubella syndrome is highly
sporadic in countries with an implemented routine rubella immunization program. According to WHO estimates, global rubella vaccination coverage was
69% by 2018 [32]. The lowest vaccination rates are detected in African and
South-East Asian regions, where congenital rubella infection rates are high,
expectedly [32, 33].
The fetus’s most severe damage is caused by maternal rubella infection during
the rst trimester. The risk of major fetal defects is very low in maternal infections
contracted after the 16th week of pregnancy. However, some clinical manifestations
like SNHL may occur in late maternal infections up to the 20th week of gestation.
Congenital rubella syndrome may affect almost every system of the fetus, including
ophthalmologic, cardiac, neurologic, and auditory structures. Clinical manifestations may appear at birth or later in life as a late-onset sequela. Early manifestations
may be transient or permanent [34, 35].
Sensorineural HL, primarily bilateral, is a common clinical manifestation in congenital rubella infection, detected in up to one-half to two-third of infants. The hearing may be affected permanently at birth or later in childhood. Since there is no
effective specic treatment for rubella, supportive treatment and rehabilitation are
warranted [3, 35].
3.4.1.4 Congenital Syphilis andHearing Loss
Treponema pallidum, a gram-negative spirochete bacterium, is the causative agent
of syphilis. It may be acquired by sexual contact leading to acquired syphilis, or by
transplacental transmission from mother to fetus leading to stillbirth, prematurity, or
congenital syphilis. The incidence of congenital syphilis is closely related to the rate
of syphilis in women of childbearing age [36]. The incidence of syphilis is on the
rise, increasing the number of congenital syphilis. According to WHO estimates,
approximately 3% (1–11%) of childbearing women are found to be positive for
syphilis in 78 countries [37]. A meta-analysis found that congenital syphilis can
develop in 15% of infants of untreated mothers with syphilis [38].
Congenital syphilis can present with early (<2years of age) and late (≥2years of
age) manifestations. Sensorineural HL, mostly sudden, severe, and bilateral, is associated with late congenital syphilis. The famous Hutchinson’s triad of HL, notched
incisors, and interstitial keratitis is historically accepted as pathognomonic for late
congenital syphilis [36, 39]. The rate of SNHL in late congenital syphilis has been
reported as about 10–15%. Once established, syphilitic HL is not responsive to
specic antibiotic treatment. However, if congenital syphilis is diagnosed and
treated appropriately in the neonatal period, SNHL can be prevented [40]. More
importantly, congenital syphilis can be prevented by early and appropriate treatment
of infected pregnant women detected by early screening.
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Acquired syphilis can also result in HL, albeit rarer in children than adults.
Otosyphilis, a congenital and acquired syphilis complication, may cause bilateral or
unilateral SNHL with sudden onset or progressive HL.Tinnitus and vertigo may
accompany hearing impairment, which may be the initial presentation. Therefore,
syphilis should be considered in the differential diagnosis of any sexually active
patient with sudden or uctuating HL or vestibular symptoms. Hearing loss may
persist despite therapy [3, 36, 39, 41].
H. Aktürk et al.
3.4.1.5 Congenital Zika Virus Infection andHearing Loss
Zika virus is a avivirus transmitted by mosquitoes to humans. It may also spread
among human beings through sexual and vertical transmissions and blood product
transfusion. Zika virus has a geographic preference for Africa, Southeast Asia, the
Pacic Islands, the Americas, and the Caribbean. Although discovered in 1947, the
Zika virus was recognized globally in 2015–2016, when it caused an outbreak in the
Americas, the Caribbean, and the Pacic region [42, 43]. In 2016, the devastating
consequences of the Zika virus infection during pregnancy on the developing fetus
causing congenital birth defects, including microcephaly, were discovered [42, 44].
Since distinctive congenital anomalies were observed in infants of mothers with
Zika virus infection, a denition for congenital Zika virus syndrome (CZS) was
established. Clinical manifestations of CZS may show a variable intensity and
mainly include intrauterine growth retardation, microcephaly, craniofacial disproportion, neuromotor abnormalities, seizures, arthrogryposis, ocular abnormalities,
cardiac anomalies, and SNHL [43, 44]. Hearing impairment has been reported in
approximately 6–7% of infants with in-utero Zika virus exposure, ranging from
zero to 17% [43, 45, 46]. It is prominently more frequent in infants with microcephaly reaching up to 75% with a 14-fold increased risk for SNHL [45]. However,
since hearing impairment may also be observed in asymptomatic or mildly symptomatic cases, all exposed newborns should be screened for hearing [44, 45].
3.4.1.6 Herpes Simplex Virus Infection andHearing Loss
Herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) are enveloped, doublestranded DNA viruses belonging to the Herpesviridae family. As in other herpes
viruses, HSV develops latency after primary infection. The virus may be shed in
primary infection or reactivation regardless of symptomatology. Herpes simplex
virus infection is transmitted by intimate contact through inoculation of mucocutaneous sites by infected body secretions. It can be transmitted from the infected
mother to the fetus or neonate in three different periods; intrauterine (congenital
infection), perinatal (perinatal infection, natal infection), and postnatal (postnatal
infection). Intrauterine HSV infection is rarely seen and causes a different clinical
picture than perinatal (natal) and postnatal infections, which may include cutaneous
scars, limb hypoplasia, diffuse brain damage, microcephaly, and ocular ndings.
Perinatal and postnatal HSV infections may present with disseminated infection,
infection localized to the CNS, and infection localized to the skin, eye, or mouth
(SEM). Asymptomatic neonatal infection is rarely seen. Although there is limited
evidence for a causal relationship, HSV infections, especially those affecting the
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CNS, may lead to SNHL [39, 47]. In utero HSV infections or perinatal and postnatal
HSV meningitis or encephalitis are accepted as risk factors for SNHL development,
and monitoring hearing is recommended for those infants [48, 49].
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3.4.1.7 Neonatal Sepsis andMeningitis andHearing Loss
Meningitis and culture-positive sepsis are risk factors for hearing impairment in the
neonatal period [49, 50]. In a recent meta-analysis, the prevalence of hearing impairment in neonatal populations of middle- and high-income countries was 2.21 per
1000 [9]. Expectedly, it was much more common and more likely to be bilateral in
infants managed in neonatal intensive care units (NICUs) due to risk factors like
infections, hypoxia, intracranial hemorrhage, hyperbilirubinemia, and ototoxic
drugs [9]. Coenraad etal. [50] determined that sepsis and meningitis are risk factors
for SNHL in NICU infants. For infants hospitalized in the rst month of life for a
condition associated with potentially elevated hearing thresholds like culturepositive sepsis, even if they had a normal newborn hearing screening, a new hearing
evaluation before discharge is recommended [49].
3.4.2 Focal andSystemic Infectious Diseases
3.4.2.1 Otitis Externa inChildren andHearing Loss
Otitis externa is dened as inammation of the external ear canal. It is predominantly caused by bacterial infections, facilitated by a breakdown of local defense
mechanisms. Risk factors include increased moisture, trauma, foreign body, dermatitis, and viral infections. Conductive HL is among the symptoms of otitis externa,
together with otalgia, itching, and fullness. Hearing loss is expected to resolve after
the relief of inammation. Although erythema of the external ear canal may involve
the TM, otitis externa should be differentiated from acute otitis media (AOM) since
both have different treatment modalities. Treatment of external otitis mainly consists of ototopical therapy. Topical drops with ototoxic potential, like aminoglycosides and alcohol, should not be applied in patients with a suspicion of nonintact
TM.Ear candles may also induce a risk of HL and should not be used in treating
otitis externa [51–53].
3.4.2.2 Acute Otitis Media inChildren andHearing Loss
Otitis media is a broad term referring to inammation of the middle ear. It covers
several entities like AOM, otitis media with effusion, chronic otitis media with effusion, and chronic suppurative otitis media. Acute otitis media, also called suppurative otitis media, is dened as an acute bacterial infection of the middle ear uid. It
is a prevalent childhood disease, mainly in the rst 3years of age, causing high
numbers of healthcare visits and antibiotic consumption. Symptoms may include
fever, ear pain, ear drainage, and HL.
When the middle ear space is lled with uid, whether infected or not, HL
ensues. Perforation of the TM and the erosion of middle ear ossicles may also occur
in AOM and interfere with the transmission of sound vibrations due to uid
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accumulation, resulting in CHL [4, 54]. On the other hand, studies have demonstrated the presence of a sensorineural component in a considerable number of
patients with AOM ranging between 2.4 and 10.6% and up to 43.3% in a tertiary
care hospital [55, 56]. Even during the early course of uncomplicated AOM, alteration in cochlear function has been observed [55]. It is thought that inammatory
mediators and toxins passing from the middle ear to the inner ear through the round
window may lead to cochlear inammation, leading to SNHL [55–57].
H. Aktürk et al.
3.4.2.3 Otitis Media withEffusion inChildren andHearing Loss
Otitis media with effusion can be dened as the presence of uid in the middle ear
without any symptoms and signs of inammation [54]. Negative pressure is built up
in the middle ear when the eustachian tubes are blocked primarily due to an upper
respiratory tract infection. The uid in the middle ear can lead to a mild to moderate
HL, the most common complication of otitis media with effusion [54, 58]. Hearing
sensitivity and speech perception may be affected, leading to speech impairment in
the growing child [58, 59]. Hearing loss is reversible if the uid in the middle ear is
resolved. Since otitis media with effusion has a chance of spontaneous resolution,
watchful waiting is an option in the management. The persistence of otitis media
with effusion for 3–6 months associated with HL indicates tympanostomy tube
insertion [54, 60].
3.4.2.4 Recurrent Otitis Media inChildren andHearing Loss
The resurgence of all clinical ndings related to AOM after successful treatment and
relief of signs and symptoms is recurrent AOM. Placement of PE tubes may be
considered for managing children with recurrent otitis media, dened as three or
more AOM episodes in 6months or 4 within 12months with at least one episode
during the preceding 6months [54, 61]. Recurrent AOM in childhood is associated
with adult HL [62]. Prophylactic antibiotics are not recommended in patients with
recurrent AOM due to a lack of effectiveness and increased rates of antibiotic resistance [63]. Tympanostomy tubes may be helpful if there is middle ear effusion.
Otherwise, they are not recommended due to increasing the risk of structural
changes in the TM, which may lead to reduced hearing [61, 62].
3.4.2.5 Mastoiditis inChildren andHearing Loss
Mastoiditis can be a complication of AOM. Mastoiditis can be acute or chronic,
which may lead to HL.Both CHL and SNHL may ensue due to mastoiditis. In the
early phase of infection, hearing impairment may be reversible. However, chronic
mastoiditis may end up with irreversible HL [64].
3.4.2.6 Bacterial Meningitis, Viral Meningitis, andHearing Loss
As in the neonatal period, bacterial meningitis and viral meningitis may end with
hearing impairment. It is thought that inammation during meningitis may spread
to inner ear structures, causing labyrinthitis and cochlear damage. Inammation or
ischemia of the auditory nerve may also be another mechanism of hearing impairment in meningitis [4]. Hearing loss is the most common signicant sequela after
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bacterial meningitis, followed by cognitive decits, seizures, and motor decits [3,
65–68]. In some patients, hearing impairment may be temporary and resolve after a
while [68, 69].
Hearing impairment is the highest after pneumococcal meningitis, followed by
Haemophilus inuenzae type b (Hib) meningitis and meningococcal meningitis,
both of which have comparable rates [67]. Bacterial meningitis prevalence has
decreased dramatically following the introduction of conjugate vaccines, effective
against the three most common bacterial etiologies. Haemophilus inuenzae type b
meningitis has been nearly eradicated in places where routine administration of the
Hib conjugate vaccine has been implemented. Pneumococcal and meningococcal
conjugate vaccines have also signicantly reduced rates of associated bacterial
meningitis [66, 69].
Patients with viral meningitis have more favorable outcomes compared with bacterial meningitis. Hearing loss can occur following viral meningitis, although it is
seen far less frequently than bacterial meningitis [70].
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3.4.2.7 Recurrent Meningitis, Congenital Defects, andHearing Loss
Recurrent meningitis may result from cerebrospinal uid (CSF) leak from the ear,
namely otorrhea. A cerebrospinal uid leak may occur posttraumatic, iatrogenic,
i.e., after surgery, or spontaneously. Spontaneous CSF leak is a rare condition
caused by congenital inner ear defects, creating abnormal communication between
the subarachnoid space and the tympanomastoid cavity. Failure of cochlear development during fetal life may end with various inner ear malformations, like
Mondini’s dysplasia, associated with hearing impairment. Before recognizing inner
ear defects, meningitis occurring due to these defects was thought to be the reason
for HL seen in these children. In children with recurrent meningitis, a search should
be undertaken for a probable inner ear deformity causing both SNHL (especially
unilateral SNHL) and an abnormal CSF stula. Temporal bone computed tomography is the preferred method for detecting inner ear deformities, and surgical closure
is the choice of treatment to prevent recurrent meningitis, together with appropriate
vaccination [71–73].
3.4.3 Bacterial Infections inChildren andHearing Loss
The leading bacterial infections associated with HL are AOM, its local suppurative
complications, and bacterial meningitis. Besides these above-mentioned bacterial
etiologies, tuberculosis is a commonly seen disease with a relatively rare connection
with HL.Mostly antituberculosis drug regimens are associated with hearing impairment [74]. Acute SNHL due to tuberculous meningitis has been reported [75].
Tuberculosis of the middle ear is a rare form of the disease leading to hearing difculties [75, 76].
Some other bacterial infections are rarely reported as the etiology of hearing
impairment. Lemiere’s syndrome refers to septic thrombophlebitis of the internal
jugular vein that typically begins as an oropharyngeal infection and is usually
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caused by Fusobacterium spp. There are reports describing patients with SNHL
caused by otogenic Lemiere disease [77]. Epidemic typhus, a louse-borne infection,
is caused by an obligate, intracellular, gram-negative coccobacillus Rickettsia
prowazekii. Hearing loss is a CNS manifestation of epidemic typhus [78, 79].
Whipple disease, caused by Tropheryma whipplei, a gram-positive bacillus, is a rare
systemic bacterial infection transmitted mainly by the fecal–oral route. Hearing loss
is among the CNS symptoms and signs of Whipple disease [80].
H. Aktürk et al.
3.4.4 Viral Infections inChildren andHearing Loss
Several viral infections are associated with HL, including CMV, Epstein Barr virus
(EBV), HSV, varicella zoster virüs (VZV), measles virus, mumps virus, rubella
virus, lymphocytic choriomeningitis virüs (LCMV), human immunodeciency
virus (HIV), and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
infections. These infections are associated with SNHL, which may be congenital or
acquired, unilateral or bilateral, mild or severe. Viruses can impair hearing by
directly damaging the inner ear structures, inducing a host-mediated inammatory
response, or facilitating bacterial or fungal infections [65]. Some viral infections
have appropriate antiviral treatment, which may reverse or limit HL.Some others
have effective vaccines against them, preventing the disease with a potential for
hearing impairment [48].
Cytomegalovirus and rubella virus infections can cause congenital HL, as mentioned above. Lymphocytic choriomeningitis virus, a rarely seen single-stranded
RNA virus transmitted to humans by secretions of rodents, may also lead to congenital HL if contracted during early pregnancy, together with visual impairment
and microcephaly [81]. Herpes simplex viruses may cause both congenital and
acquired HL.Beyond infancy, HL is associated with HSV meningitis or encephalitis in most cases. Antiherpetic drugs and sometimes steroids are used to ameliorate
HL and other ndings related to HSV infections [39, 48].
Human immunodeciency virus may lead to HL in about 30% of HIV-infected
people, both in children and adults, although the risk increases with age. Infants
with in-utero exposure to HIV may also develop hearing impairment. Auditory
involvement may be unilateral or bilateral, progressive or sudden, conductive or
sensorineural. The pathogenesis can be related to many factors, including direct
effects of the virus, increased susceptibility to infections of the middle ear and CNS,
and ototoxic drugs used in treatment [39, 48, 82].
Varicella zoster virus remains latent in various ganglions after primary infection.
Reactivation of the VZV within the geniculate ganglion affects the seventh and
eighth cranial nerves. It results in herpes zoster oticus or Ramsey Hunt syndrome
with a clinical picture of herpetic vesicles, facial nerve paralysis, SNHL, and otalgia. Rarely the rash may be absent. Treatment involving antiherpetic agents and
steroids may improve HL more frequently than facial nerve palsy [39, 48, 83].
Before widespread vaccination, measles was an important cause of HL, accounting for 5–10% of cases with profound HL [84]. It is still an important reason for HL
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in areas with low vaccination rates. In a study conducted in Nigeria between 2009
and 2018, measles was detected as the cause of profound SNHL in 45.8% of 142
children [85].
Mumps infection generally presents as a u-like illness and bilateral parotitis
and may induce occasional and well-known complications like pancreatitis, orchitis, aseptic meningitis, encephalitis, and SNHL, mostly unilateral. Incidence of
SNHL ranges from approximately 1 per 1000 to 1 per 20,000 mumps cases.
Hearing impairment may develop following mumps infection with or without
meningitis, encephalitis, or even after an asymptomatic infection. Although spontaneous recovery may be seen in mild to moderate cases, profound SNHL following the mumps infection seems refractory to various treatments, including steroids
[3, 39, 48, 86].
Acute EBV infection has been rarely reported as a cause of sudden SNHL and is
assumed to be related to cranial nerve involvement [3, 87, 88]. Finally, coronavirus
disease 2019 (COVID-19) caused by SARS-CöV-2 infection has been linked to the
SNHL in a number of recent reports [89, 90].
3.5 Conclusion
Hearing impairment is a common health issue in childhood; however, it may go
unnoticed and result in language and social development problems since hearing is
essential in communication and engagement with others. Although the exact cause
is not always possible to determine, understanding and awareness of the etiology are
necessary since a crucial part of the causes are preventable. Infections have an
important role in hearing impairment. Some strategies may be held to prevent the
occurrence of infectious causes, like strengthening the immunization programs for
children and women of childbearing age, implementing antenatal screening of some
infections during pregnancy, and training healthcare workers about ear diseases and
their relevance to HL.If the cause of HL cannot be prevented, every effort should be
made for early identication, treatment, and rehabilitation of children with HL.
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